A CORRELATIONAL STUDY BETWEEN COUPLING INTERVAL RATIO AND SYMPTOMS IN PATIENTS WITH IDIOPATHIC VENTRICULAR PREMATURE COMPLEXES IN 24 HRS HOLTER MONITORING

Background and objective:Ventricular premature complexes (VPCs) are the most common arrhythmia encountered in cardiology OPD. Patients with frequent VPCs are often symptomatic. Our study aims to identify the ECG predictors of symptoms in patients with idiopathic VPCs in 24 hours Holter monitoring. Subjects and methods: This study was conducted on 102 patients with VPCs during the period of February 2019 to December 2019 in cardiology OPD of our centre.All the patients were screened with transthoracic echocardiography.24 hours Holter monitoring was done, the measured parameters were QRS width (Both in sinus beat & VPC), coupling interval (CI),CI ratio (CL/sinus cycle length) and VPC burden (Number and percentage of VPCs per day). Results:Both group had similar categorical age group and gender.ORS width of both sinus beat (P = 0.389) and VPCs (P = 0.035), VPC CI (P=0.487) and VPC burden (P = 0.458) did not correlate with symptoms but VPC CI ratio were significantly higher in Group B(symptomatic) than in group A (P = 0.004) Conclusion:There is a relationship between VPC related symptoms and VPC CI ratio.

A Plasma-Based, Amiodarone-Impregnated Material Decreases Susceptibility to Atrial Fibrillation in a Post–Cardiac Surgery Model

Objective This study aimed to test the impact of a plasma-based, material (PBM) impregnated with amiodarone on atrial electrophysiology and atrial fibrillation susceptibility in a porcine post–cardiac surgery model. Methods Ten healthy pigs underwent implantation of transvenous pacing systems, after which sterile talc was infused into the pericardial sac via a pericardiotomy. In five animals, PBM was applied to the atrial epicardial surface just before talc infusion. Electrophysiologic evaluations were performed using the pacing system immediately after chest closure and 7 days later. Atrial histologic evaluations were performed. Results Immediately after chest closure, there were no significant differences in electrophysiologic parameters between talc-only and talc + PBM animals, and atrial fibrillation was largely noninducible. On postsurgical day 7, electrophysiologic evaluation revealed significantly shorter sinus cycle length and atrioventricular nodal refractoriness among talc-only animals relative to talc + PBM animals, possibly suggesting attenuated sympathetic nervous system activation in the latter. Atrial fibrillation inducibility and duration were significantly greater among talc-only animals. No significant differences in atrial refractoriness or conduction time between groups were apparent. Histologic evaluation revealed a relative reduction in epicardial inflammation and less myolysis among talc + PBM animals. Conclusions Epicardial application of a plasma-based, amiodarone-impregnated material was associated with a significant reduction in atrial inflammation and susceptibility to fibrillation.

Rate Control in Atrial Fibrillation by Cooling: Effect of Temperature on Dromotropy in Perfused Rabbit Hearts

Background. Cooling has emerged as a therapeutic option in critically ill patients (especially after cardiac resuscitation) and might also have a negative dromotropic effect in atrial fibrillation. We sought to determine the impact of cooling on electrophysiologic properties of Langendorff-perfused rabbit hearts.Methods and Results. In 20 isolated Langendorff-perfused rabbit hearts, the temperature of the tissue bath was changed between 17 and 42°C. With decreasing temperature, significant increases of the spontaneous sinus cycle length, decreases of the mean ventricular heart rate during atrial fibrillation, and relevant increases of atrial and ventricular refractory periods were observed (ANOVAP<.01).Conclusions. Cardiac hypothermia leads to a significant drop of mean ventricular heart rate during atrial fibrillation. Negative chronotropy and dromotropy induced by moderate cardiac hypothermia might be a feasible therapeutic approach in patients with hemodynamically relevant tachyarrhythmias in a CCU/ICU setting.

Prevention of diminished parasympathetic control of the heart in experimental heart failure

Decreased synaptic transmission in parasympathetic ganglia contributes to abnormal parasympathetic function in heart failure (HF). Because nicotinic ACh receptors (nAChR) mediate synaptic transmission at the ganglion and upregulate in response to chronic exposure to agonist in vitro, we tested the hypothesis that repeated exposures of ganglionic neurons to a nAChR agonist can prevent a loss of parasympathetic control in HF. Two sets of experiments were performed. In set 1, unpaced control dogs and dogs undergoing pacing-induced HF were treated with a repeated intravenous nicotinic agonist during the development of HF. Under conditions of sympathetic blockade, R-R responses to a bolus injection of 200 μg 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP; nicotinic agonist) were found to be increased five times over the untreated group after 6 wk. In experimental set 2, dogs treated with weekly DMPP injections and in HF were anesthetized and underwent electrical stimulation of the right vagus nerve, which showed sinus cycle length responses >10 times that of controls ( P < 0.05). Complete ganglionic blockade with hexamethonium abolished all responses, confirming that synaptic transmission was mediated entirely by nAChRs in both controls and HF. Despite decreased ganglionic function leading to reduced parasympathetic control of the heart in HF, repeated exposure with a nicotinic agonist during the development of HF results in not only preserved but also supranormal effects of parasympathetic stimulation on the sinus node.

Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats

Paraplegia may increase susceptibility to ventricular arrhythmias by altering the autonomic control of the heart. Altered cardiac autonomic control has been documented to change the expression of genes that encode cardiac Ca2+ regulatory proteins. Therefore, we tested the hypothesis that paraplegia alters cardiac electrophysiology with concomitant changes in Ca2+ regulatory proteins in a manner that increases the susceptibility to ventricular arrhythmias. To test this hypothesis, intact ( n = 10) and paraplegic ( n = 6) male Wistar rats were chronically instrumented to measure atrioventricular (AV) interval, sinus cycle length, sinus node recovery time (SNRT), SNRT corrected for spontaneous sinus cycle (cSNRT), Wenckebach cycle length (WCL), and the electrical stimulation threshold to induce ventricular arrhythmias. In addition, relative protein abundance and mRNA expression for sarco(endo)plasmic reticulum Ca2+ ATPase (SERCA), phospholamban, and the Na/Ca exchanger were determined in intact ( n = 8) and paraplegic ( n = 8) rats. Paraplegia significantly ( P < 0.05) reduced AV interval (–25%), sinus cycle length (–24%), SNRT (–28%), cSNRT (–53%), WCL (–19%), and the electrical stimulation threshold to induce ventricular arrhythmia (–48%). Paraplegia significantly increased the relative protein abundances of SERCA (45%) and the Na/Ca exchanger (40%) and decreased phospholamban levels (–28%). In contrast, only the relative mRNA expression of the Na/Ca exchanger was increased (25%) in paraplegic rats. These data demonstrate that paraplegia enhances cardiac electrophysiological properties and alters Ca2+ regulatory proteins in a manner that increases susceptibility to ventricular arrhythmias.

Slow rate during AF improves ventricular performance by reducing sensitivity to cycle length irregularity

Atrial fibrillation (AF) is characterized by short and irregular ventricular cycle lengths (VCL). While the beneficial effects of heart rate slowing (i.e., the prolongation of VCL) in AF are well recognized, little is known about the impact of irregularity. In 10 anesthetized dogs, R-R intervals, left ventricular (LV) pressure, and aortic flow were collected for >500 beats during fast AF and when the average VCL was prolonged to 75%, 100%, and 125% of the intrinsic sinus cycle length by selective atrioventricular (AV) nodal vagal stimulation. We used the ratio of the preceding and prepreceding R-R intervals (RRp/RRpp) as an index of cycle length irregularity and assessed its effects on the maximum LV power, the minimum of the first derivative of LV pressure, and the time constant of relaxation by using nonlinear fitting with monoexponential functions. During prolongation of VCL, there was a pronounced decrease in curvature with the formation of a plateau, indicating a lesser dependence on RRp/RRpp. We conclude that prolongation of the VCL during AF reduces the sensitivity of the LV performance parameters to irregularity.

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Depressed parasympathetic tone is associated with an increased risk of sudden cardiac death. Exercise and the postexercise recovery period, which are associated with parasympathetic withdrawal, are high risk periods for sudden death. However, parasympathetic effects on cardiac electrophysiology during exercise and recovery have not been described. Electrophysiology studies were performed using noninvasive programmed stimulation (NIPS) in nine subjects (age 59 ± 18 yr) with implanted dual-chamber devices and normal left ventricular function during multiple bicycle exercise sessions. NIPS was performed at rest, during exercise, and in the early recovery period both before and after parasympathetic blockade with atropine. Parasympathetic effect was defined as the value of the parameter of interest in the absence of atropine minus the value of the parameter in the presence of atropine. During exercise, sinus cycle length, atrioventricular (AV) block cycle length, AV interval, and ventricular effective refractory period shortened; in recovery, the values were intermediate between the rest and exercise values ( P < 0.0001 by ANOVA). Parasympathetic effects on sinus cycle length, AV block cycle length, AV interval, and ventricular effective refractory period were 247 ± 140, 58 ± 20, 76 ± 20, and 8.6 ± 7.5 ms at rest, 106 ± 20, 37 ± 14, 24 ± 13, and 2.6 ± 7.8 ms during exercise, and 209 ± 114, 50 ± 23, 35 ± 21, and 9.5 ± 11.8 ms during recovery, respectively. There was poor correlation among the parasympathetic effects noted at the sinus node, AV node, and ventricle. Further work evaluating parasympathetic effects on cardiac electrophysiology during exercise and recovery in patients with heart disease is required to elucidate its role in modulating the risk of sudden cardiac death noted at these times.